Hypoxia is a common occurrence following stroke and associated with poor clinical and functional
outcomes. Normal oxygen physiology is a finely controlled mechanism from the oxygenation of haemoglobin in the
pulmonary capillaries to its dissociation and delivery in the tissues. In no organ is this process more important than
the brain, which has a number of vascular adaptions to be able to cope with a certain threshold of hypoxia, beyond
which further disruption of oxygen delivery potentially leads to devastating consequences. Hypoxia following stroke
is common and is often attributed to pneumonia, aspiration and respiratory muscle dysfunction, with sleep apnoea
syndromes, pulmonary embolism and cardiac failure being less common but important treatable causes. As well as
treating the underlying cause, oxygen therapy is a vital element to correcting hypoxia, but excessive use can itself
cause molecular and clinical harm. As cerebral vascular occlusion completely obliterates oxygen delivery to its target
tissue, the use of supplemental oxygen, even when not hypoxic, would seem a reasonable solution to try and correct
this deficit, but to date randomised clinical trials have not shown benefit.

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• Hypoxia after stroke: a review of experimental and clinical evidence